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56 Cards in this Set

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Rifamate
-Isoniazid 150mg
-Rifampin 300mg
Rifater
-Isoniazid 50mg
-Rifampin 120mg
-Pyrazinamide 300mg
Drug Activity vs Fast Growing TB Subpopulations
INH>RFM>STR>others (quinolones/EMB)
Drug Activity vs Slow Growing TB Subpopulations
PZA>INH>RFM
First Line Agents vs. TB
-Isoniazid (INH): IV/PO
-Rifampin (RFM): IV/PO
-Pyrazinamide (PZA): PO
-Ethambutol (EMB): PO
-Streptomycin (STR): IM
Fluoroquinolone MOA
-inhibition of topoisomerase II, aka DNA gyrase (gram -), and topoisomerase IV (gram +)
-bacteriacidal
Mechanism of Resistance vs. Fluoroquinolones
-alterations of amino acid sequences which change base pairs of DNA decreasing the affinity for drug binding
-DNA gyrase (topoisomerase II) & topoisomerase IV mutations
-decreased intracelluar accumulation
Fluroquinolone Gram - Activity
-E. coli
-Enterobacteriaceae (E. coli, Klebsiella pneumoniae, Serratia marescens, Salmonella sp.)
-Pseudomonas aeruginosa
-Haemophilus influenzae
-Moraxella catarrhalis
-Neisseria gonorrhea
Fluroquinolone Limited Gram + Activity
-Streptococcus pneumoniae
-Staphylococcus aureus
-Enterococci sp.
Fluroquinolone Expanded Gram + Activity (Levofloxacin, Moxifloxacin, Gemifloxaxin)
-PCN-R Streptococcus pneumoniae
-Streptococcus pyogenes
-Atypicals (Legionella sp., Mycoplasma pneumoniae, Chlamydia pneumoniae)
Fluoroquinolone Anaerobic Activity (Levofloxacin, Moxifloxacin)
-Bacteroides fragilis
-Provetella sp.
-Fusobacterium sp.
-Peptostreptococcus sp.
-Clostridium sp.
DNA Gyrase (Topoisomerase II) Mutations
-gyr A
-gyr B
Topoisomerase IV Mutations
-par C
-par E
Reasons for Decreased Intracellular Fluoroquinolone Accumulation
-reduced penetration thru cell wall
-active efflux
Use of Fluoroquinolones
-UTI (not moxifloxacin)
-cSSSI
-Infectious diarrhea
-Urethral/cervical infections
-Prostatis
-Acute sinusitis
-Acute exacerbations of chronic bronchitis
-Community acquired pneumonia
Systemic Mycoses (Endemic Fungi)
-Histoplasmosis (Histoplasma capsulatum)
-Blastomycoses (Blastomyces dermatophytosis)
-Coccidioidomycosis (Coccidioides immitis)
Opportunistic Systemic Mycoses
-Candidiasis (yeast)
-Cryptococcosis (yeast)
-Aspergillosis (mould)
-Zygomycoses (mould)
Polyenes MOA
binds to ergosterol (more avidly then cholesterol), causing intercalation of cell membrane allowing leakage of intracellular cations
When would you use Amphotericin B po?
decontaminate gut prior to surgery
Amphotericin B Resistance
-Candida lusitaniae
-Aspergillus terreus
-Scedosporium sp.
-(+/-) Fusarium
-Zygomycosis
Distribution of Amphotericin B to Tissue
kidney>liver>spleen>lung>
heart>skeletal muscles>brain>bone>CSF>eye
Azole MOA
inhibition of 14-alpha-demethylase causes inhibition of ergosterol synthesis resulting in accumulation of toxic sterols in the cell membrane
Echinocandins MOA
inhibition of beta-1,3 glucan synthase causing inhibition of beta- 1,3 & beta-1,6 glucans synthesis causing fungal cell walls to become structurally abnormal and susceptible to osmotic stress
Isoniazid MOA
acylates NADH and prevents if from reducing alkene in FA synthesis ultimately blocking mycolic acid synthesis and disrupting the cell wall
Rifampin MOA
inhibits DNA-dependent RNA polymerase (DDRP):
-π-π bonding between naphthalene & aromatic amino acids of DDRP
-chelation to Zn present in DDRP (OH @ C1 & C8)
-hydrogen bonding to enzyme (OH @ C21 & C28)
Ethambutol MOA
-inhibition of arabinosyl transferase which ultimately inhbits LAM and AG destroying integrity of cell wall
-blocks RNA synthesis
Pyrazinamide MOA
-lowers pH of media
-antimetabolite of NAD synthesis which is necessary for FA synthesis
-inhibits the gene that endocdes for FA synthase I thus inhibiting FA synthesis
Streptomycin MOA
inhibits protein synthesis by binding to the 30S ribosomal subunit
Causes of Community Acquired Pneumonia
1. Streptococcus pneumoniae
2. Haemophilus influenzae
3. Moraxella catarrhalis
Capsid Virus
-capsid
-environmentally stable
-released via cell lysis
-easily spread via oral or fecal route
-can dry out & retain infectivity
-can survive GI
-elicit protective antibody response
Envelope Virus
-envelope membrane
-environmentally liable
released via cell lysis & budding
-must stay wet to remain infectious
-do not survive GI
-spread via blood, body secretions, & transplants
-elicit cell-mediated immune response or hypersensitivity & inflammation response
Uncoating Inhibitors MOA
neutralize and inhibit Influenza A viral uncoating preventing virus from penetrating host cells
Ribavirin MOA
causes alteration of cellular nucleotide pools and inhibition of viral mRNA synthesis
"Cyclovirs" MOA
activated via viral thymidine kinase and converted to a triphosphate derivative that inhibits DNA synthesis & viral replication by competeing with deoxyguanosine triphosphate for viral DNA polymerase becoming incorporated into vral DNA causing termination of DNA chain
Nucleoside Analogs MOA
inhibition of viral DNA replication similar to "Cyclovirs" with different nucleotide derivatives
Non-Nucleosie Analogs MOA
directly inhibits DNA polymerase
Neuraminidase Inhibitors MOA
N-acetylneuraminic acid (sialic acid) analog that inhibits viral neuraminidases & leaves uncleaved sialic acid residues on the surfaces of the host cells and influenza viral envelopes. Viral hemagglutinin binds these residues resulting in a viral aggregation at the host cell & a reduction in the amount of virus that is released to infect other cells.
Interferons & Immunoglobulins MOA
inhibition of viral penetration or uncoating, synthesis of mRNA, translation of viral proteins, &/or viral assembley and release
Sulfonamides MOA
antimetabolite of PABA
Trimethoprin MOA
antimetabolite of dihydrofolic acid that inhibits dihydrofolate reductase
Nitrofurans MOA
-inhibits acetyl-CoA thereby interfering with carbohydrate metabolism
-dirsupts bacterial cell wall formation
Methenamine MOA
causes denaturation of proteins by forming a Schiff base
Fosfomysin MOA
-analog of fosfoenopyruvate that acts as a false substrate of transferase and inhibits peptidoglycan and cell wall synthesis
-decreases affinity of bacteria to cell wall (?)
Phenazopyridine MOA
urinary analgesic with NO antimicrobal properties
Undecylenic Acid MOA
alters membrane and conditions needed for fungal growth
Talnaftate MOA
blocks the oxidation of squalene to squalene epoxidase and ultimatley the formation of ergosterol
Allylamines MOA
interfere with ergosterol synthesis by blocking squalene-2,3 epoxidase
Ciclopirox MOA
-blocks fungal transmembrane transport
-interferes with DNA & RNA synthesis
Griseofulvin MOA
inhibits mitosis by interacting with microtubules causing disruption of the mitotic apparatus arresting metaphase
Flucytosine MOA
inhibits DNA synthesis by inhibiting thymidylate synthase which converts uracil into thymine
MAC drug therapy
-Macrolides (Clarithroymcin, Azithromycin)
-Refabutin
-Ethambutol
-Ciprofloxacin
-Clofazimine
Ethionamide MOA
acylated InhA (NAD) leading to inhibition of FA synthesis
Para-aminosalicylic acid (PAS) MOA
antimetabolite of PABA
Cycloserine MOA
inhibitor of L-alanine racemase that converts L-alanine into D-alanine ultimately inhibiting synthesis of peptidoglycan needed for the cell wall
Capreomycin MOA
inhibits protein synthesis by binding to the 50S ribosomal subunit
Kanamycin MOA
inhibits protein synthesis by binding to the 30S ribosomal subunit